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At least 19 recordsLinked to original sources
PubMed1975

A study of the immuno-suppressive activity of Herpes simplex virus type 2 and the tumor enhancing potential of the virus on Yoshida sarcoma.

The relative delays of Yoshida sarcoma (YS) tumor induction were used as indicator for the immunosuppressive potential caused by the subcutaneous infection of Sprague-Dawley rats with approximately 10(7) TCD50 HSV-2. The tumor formation is clearly accelerated and the number of tumors is increased as compared to sham injected rats. The impairment of immunity is at its maximum when the virus and the YS cells are applied simultaneously, whereas virus given after the tumor is of no consequence. The adoptive neutralization test of Winn showed that the neutralization potential of spleen cells originating from HSV-2 infected donors is decreased from day 8 to day 11 post infection but rturns back to normal a week later. The stimulation of spleen cells with PHA is reduced up to 50% of control values on day 6 to 8 post virus infection but PFC and RFC values are not noticeably affected and neither are the hemagglutination titres. The implications of the immuno-suppressive faculty of HSV-2 for human genital malignancies are discuss.ed.

Animals↗
PubMed1975

An experimental postoperative metastasis system using Yoshida sarcoma inoculated subcutaneously into footpad.

When Yoshida sarcoma cells were inoculated subcutaneously into the left footpad of Donryu rats, the weight of the left lumbar lymph nodes increased proportionally to the number of the inoculated cells. Resection of primary implants the day after the inoculation of 5 x 10(6) cells failed to rescue the host rats and they died of metastases within 12 days. There was no significant difference in mean survival days between the rats (8.9 days) whose primary implants were resected on the 5th day after inoculation and the control rats (8.6 days) bearing the primary implants. Mitomycin-C, a highly effective drug against Yoshida sarcoma cells, produced many long survivors (over 30 days) in the treated rats whose primary implants were resected the day after inoculation, but failed to do so when resected 5 days after inoculation. All of them died of metastases within 20 days. Based on these results, this present system is discussed for its usefulness as a screening and evaluation model for antitumor agents.

Animals↗
PubMed1978

Preparation for disseminated intravascular coagulation by Yoshida sarcoma in rats.

Five days following implantation of a Yoshida sarcoma, female rats developed an increase in plasma fibrinogen concentration and a decrease in the number of platelets. The endotoxin induced fibrinisation of the microcirculation, as measured in percent involvement of glomerula, was found to be five to ten times higher than in control animals. A single injection of endotoxin without infusion was sufficient in tumor bearing animals to induce glomerular capillary thrombosis. The Yoshida sarcoma induced pathophysiological changes with a "preparative" effect on the endotoxin-induced disseminated intravascular coagulation.

Animals↗
PubMed1977

[Colorimetric studies by means of Ehrlich's reagent of blood serum of rats with Yoshida sarcoma].

Extinctions in the sera of Yoshida-sarcoma-bearing and normal rats were determined by means of a photometric measurement after the reaction of the sera with Ehrlich's reagent. Thereby the increase of the extinctions of the tumor bearers could be confirmed, also being found in tumor patients. The difference in terms of normal animals was statistically significant. The supposed relations between the exitation of the extinctions and the level of glycoproteins could be supported by correlating calculations.

Animals↗
PubMed1979

Influence of charge on the inactivation of membrane bound (Na+ + K+)-ATPase of Yoshida sarcoma cells by inhibitor proteins from cobra venom.

Inactivation of (Na+ + K+)-ATPase of Yoshida sarcoma cells and beef brain microsomes by phospholipase A2 and a cytotoxin P6 from snake venom has been examined in relation to their activity to degrade phospholipids. Cytotoxin P6 which was most basic and devoid of phospholipase activity was most effective in inhibiting the (Na+ + K+)-ATPase of Yoshida sarcoma cells. Phospholipase A2 from Naja naja which was most active in degrading phospholipids was least effective in inhibiting (Na+ + K+)-ATPase in Yoshida sarcoma cells or in beef brain microsomes. Addition of trace amounts of cytotoxin P6 to the phospholipase considerably enhanced the inactivation of (Na+ + K+)-ATPase. The evidence suggests that the charge of the inhibitor protein and its specific structure play an important role in the inactivation of (Na+ + K+)-ATPase.

Animals↗
PubMed1977

A new deoxyuridine-5'-triphosphatase in Yoshida sarcoma cells involved in deoxyuridine 5'-triphosphate metabolism.

A magnesium-independent deoxyuridine-5'-triphosphatase was found in Yoshida sarcoma cells but not in normal rat liver. The phosphatase is specific for deoxyuridine 5'-diphosphate and deoxyuridine triphosphate, and its Km for deoxyuridine triphosphate is 2.7 X 10(-7) M. The enzyme was not inhibited by fluoride and required no divalent cations. Thus it differs from known nucleotide phosphatases. Deoxyuridine monophosphokinase, which is detectable in a crude extract of normal rat liver, could not be detected in an extract of Yoshida sarcoma cells. However, with hydroxylapatite column chromatography of the extract, a deoxyuridine 5'-monophosphate kinase activity as high as that in normal rat liver was found in fractions separated from the phosphatase activity. Thus the absence of detectable deoxyuridine 5'-monophosphate kinase activity in the crude extract of Yoshida sarcoma cells is due to the presence of this nucleotide phosphatase.

Animals↗
PubMed1979

Antitumor activity of 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) and 1-(2-chloroethyl)-3-(4-methyl-cyclohexyl)-1-nitrosourea (MeCCNU) on Yoshida sarcoma ascites cells implanted into the colon wall of rats.

Three thousand Yoshida sarcoma cells were inoculated into the wall of the descending colon of each of 120 male Sprague-Dawley rats. On day 8 after the tumor implantation, the animals were at random divided into four groups of 30 rats each. The effect of cyclophosphamide (70 mg/kg), BCNU (25 mg/kg), and methyl-CCNU (45 mg/kg) after single i.p. application was investigated. The Yoshida sarcoma transplanted into the colon is sensitive to all three chemotherapeutic drugs. At the doses given cyclophosphamide showed the best results. The two nitrosoureas had a comparable antitumor activity but methyl-CCNU showed a more distinct toxic effect. The introduction of this model for testing new cytostatics in animal experiments is discussed.

Animals↗
PubMed1975

Metastasis formation of Yoshida sarcoma heterotransplanted in adult golden hamsters treated with anti-hamster thymocyte serum.

Growth of Yoshida sarcoma cells heterotransplanted in adult golden hamsters treated with antithymocyte serum was investigated. Control animals were grafted with or without hydrocoritisone conditioning. In the antithymocyte serum-treated group, tumors were produced in cheek pouches and grew progressively in size until Day 21 with no sign of regression. Little host reaction was noticed histologically around the tumor grafts throughout the course. Distant metastases were revealed at autopsy in 9 of 12 animals from Day 14 of inoculation on, and all the experimental animals died by Day 23. Six of the 9 hamsters with metastases died of tumor. By means of the back-transplantation test, the metastatic tumor cells were shown to be consistent with Yoshida sarcoma cells. In hydrocortisone-treated and untreated groups, the tumor size reached a maximum on Day 21 and Day 5, respectively, and then regression followed. No metastasis was detected in either control group.

Animals↗
PubMed1975

Instability of the duration of G1 phase of Yoshida sarcoma and ascites hepatomas.

The durations and coefficients of variance of G1, S and G2 phase were obtained for 8 cell lines of ascites tumours originated from hepatomas in rats, and these were compared. Although changes in the durations of S and G2 phases were small, the duration of G1 phase increased with the cell cycle time. The coefficient of variance of G1 phase was larger than that of S and G2 phases, most remarkedly at short cycle time. It was concluded that the G1 phase is the most unstable as well as the most variable in its duration.

Animals↗